HIPK1 Protein, Human (Sf9, GST)

HIPK1 is a multifunctional serine/threonine protein kinase that complexly regulates transcriptional control and TNF-mediated apoptosis. It acts as a corepressor for homeodomain transcription factors and regulates gene expression by phosphorylating the substrates DAXX and MYB. HIPK1 Protein, Human (Sf9, GST) is the recombinant human-derived HIPK1 protein, expressed by Sf9 insect cells , with N-GST labeled tag. The total length of HIPK1 Protein, Human (Sf9, GST) is 398 a.a., .

HIPK1, a serine/threonine-protein kinase, emerges as a multifaceted regulator involved in transcriptional control and TNF-mediated cellular apoptosis. Functioning as a corepressor for homeodomain transcription factors, HIPK1 plays a pivotal role in modulating gene expression. It phosphorylates key substrates, including DAXX and MYB, exerting regulatory control over their activities. In response to stress, HIPK1 phosphorylates DAXX, facilitating its translocation from the nucleus to the cytoplasm. Moreover, HIPK1 acts as a negative regulator of MYB by inactivating its transcription factor activity through phosphorylation. Notably, HIPK1's intricate involvement in the TNF-mediated pathway prevents MAP3K5-JNK activation in the absence of TNF, promoting apoptosis through derepression. Beyond its role in apoptosis, HIPK1 is implicated in anti-oxidative stress responses and contributes to diverse developmental processes, such as the regulation of eye size, lens formation, retinal lamination, angiogenesis, and erythroid differentiation. Furthermore, its phosphorylation of PAGE4 at 'Thr-51' is crucial for PAGE4's ability to enhance the transcriptional activator activity of JUN. This versatile kinase, HIPK1, emerges as a key player in cellular homeostasis and developmental processes with implications in pathological conditions like malignant squamous cell tumor formation.

Human

Sf9 insect cells

N-GST

Q86Z02 (T158-I555)

204851

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.